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Evidence of oxidative stress in chronic heart failure in humans
J McMurray1, M Chopra, I Abdullah
1Department of Cardiology, Western Infirmary, Glasgow, Scotland.
Insights
Oxidative stress (OS) is elevated in chronic heart failure (CHF), regardless of coronary artery disease (CAD). This study confirms OS markers are abnormal in CHF patients, indicating a need for further research into its causes and treatments.
Area of Science:
- Cardiology
- Biochemistry
- Oxidative Stress Research
Background:
- Chronic heart failure (CHF) is linked to increased oxidative stress (OS), indicated by elevated thiobarbituric reactive substances (TBARS) and reduced plasma thiol (PSH).
- It remains unclear if OS is a consequence of coronary artery disease (CAD) or CHF itself.
Purpose of the Study:
- To investigate whether OS is caused by CAD or CHF per se.
- To identify a broader range of specific OS markers that are abnormal in CHF patients.
Main Methods:
- Comparison of plasma TBARS and PSH levels in patients with CHF due to CAD versus non-CAD CHF against controls.
- Analysis of additional OS markers, including malondialdehyde, erythrocyte superoxide dismutase, caeruloplasmin oxidase, erythrocyte glutathione, and plasma conjugated dienes in CHF patients and controls.
Main Results:
- Both CAD-related CHF and non-CAD CHF groups exhibited significantly higher TBARS and lower PSH compared to controls.
- CHF patients showed elevated malondialdehyde and reduced PSH.
- Significant alterations in erythrocyte superoxide dismutase, caeruloplasmin oxidase, and erythrocyte glutathione were observed in CHF patients.
Conclusions:
- Oxidative stress is a significant factor in chronic heart failure, independent of the underlying cause (CAD or non-CAD).
- A comprehensive panel of OS markers is indeed abnormal in CHF patients, underscoring the systemic impact of oxidative damage.
Abstract:
Chronic heart failure (CHF) due to coronary artery disease (CAD) has been shown to be associated with increased plasma thiobarbituric reactive substances (TBARS) and reduced plasma thiol (PSH) concentrations, suggesting oxidative stress (OS). The aims of the present studies were (a) to determine whether OS is due to CAD or CHF per se and (b) to determine if a wider range of more specific markers of OS are abnormal in CHF. In the first study, two groups of patients (n = 15 each) were compared. Group 1 (11 male, mean age 56 years) had CHF due to CAD and group 2 (12 male, mean age 53 years) had non-CAD CHF. Median plasma TBARS in controls was 7.6 nmol.ml-1, 10.0 nmol.ml-1 in group 1 and 9.3 nmol.ml-1 in group 2 (P < 0.01 both groups vs control). Median PSH was 505 384 and 364 nmol.ml-1 (P < 0.05 and P < 0.01 vs control) respectively. Fifty-three patients with CHF were recruited in the second study. Malondialdehyde and PSH were 10.3 and 409 nmol.ml-1 respectively, compared to control values of 7.9 and 560 nmol.ml-1 (both P < 0.001). The median values for the following additional measures of OS in controls and patients were: erythrocyte superoxide dismutase 131 vs 114 U.l-1 (P = 0.005); caeruloplasmin oxidase 97 vs 197 U.l-1 (P < 0.01); erythrocyte glutathione 1.56 nmol.ml-1 vs 1.77 nmol.ml-1 (P < 0.02); plasma conjugated dienes 0.28 vs 0.33 optical density units (P = ns).(ABSTRACT TRUNCATED AT 250 WORDS)
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